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See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/293797227 Influence of supraglottic airway device placement on cerebral hemodynamics Article in Minerva anestesiologica · February 2016 CITATION 1 READS 53 8 authors, including: Some of the authors of this publication are also working on these related projects: FGFR1 and cardiomyocytes View project Sedation View project Frank Aanthony Rasulo Università degli Studi di Brescia 44 PUBLICATIONS 1,053 CITATIONS SEE PROFILE Simone Piva Spedali Civili di Brescia 25 PUBLICATIONS 189 CITATIONS SEE PROFILE Arturo Toninelli Spedali Civili di Brescia 5 PUBLICATIONS 10 CITATIONS SEE PROFILE Stefano Calza Università degli Studi di Brescia 121 PUBLICATIONS 3,265 CITATIONS SEE PROFILE All content following this page was uploaded by Simone Piva on 04 July 2016. The user has requested enhancement of the downloaded file.

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See discussions, stats, and author profiles for this publication at: https://www.researchgate.net/publication/293797227

Influence of supraglottic airway device placement on cerebral hemodynamics

Article  in  Minerva anestesiologica · February 2016

CITATION

1

READS

53

8 authors, including:

Some of the authors of this publication are also working on these related projects:

FGFR1 and cardiomyocytes View project

Sedation View project

Frank Aanthony Rasulo

Università degli Studi di Brescia

44 PUBLICATIONS   1,053 CITATIONS   

SEE PROFILE

Simone Piva

Spedali Civili di Brescia

25 PUBLICATIONS   189 CITATIONS   

SEE PROFILE

Arturo Toninelli

Spedali Civili di Brescia

5 PUBLICATIONS   10 CITATIONS   

SEE PROFILE

Stefano Calza

Università degli Studi di Brescia

121 PUBLICATIONS   3,265 CITATIONS   

SEE PROFILE

All content following this page was uploaded by Simone Piva on 04 July 2016.

The user has requested enhancement of the downloaded file.

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Influence of Supraglottic Airway Device placement on

cerebral hemodynamics

Frank RASULO, Nicola ZUGNI, Simone PIVA, Nazzareno FAGONI, Federico PE,

Arturo TONINELLI, Stefano CALZA, Nicola LATRONICO

Minerva Anestesiol 2016 Feb 09 [Epub ahead of print]

MINERVA ANESTESIOLOGICARivista di Anestesia, Rianimazione, Terapia Antalgica e Terapia Intensiva

pISSN 0375-9393 - eISSN 1827-1596

Article type: Original Paper

 The online version of this article is located at http://www.minervamedica.it

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1

Influence of supraglottic airway device placement on cerebral hemodynamics

*Frank Rasulo 1, Nicola Zugni 1, Simone Piva 1, Nazzareno Fagoni 1, Federico Pe 1,

Artuto Toninelli 1, Stefano Calza 2, Nicola Latronico 1

1Department of Anesthesiology, Intensive Care & Perioperative Medicine, Spedali Civili Hospital

of Brescia, University of Brescia, Italy; 2Department of Molecular and Translational Medicine, Unit

of Biostatistics and Biomathematics, University of Brescia, Italy

Congresses: None

Conflicts of interest: None

Funding: None

Acknowledgements: None

Corresponding Author:

Dr. Frank Rasulo

Department of Anesthesiology and Critical Care Medicine,

Spedali Civili University affiliated Hospital of Brescia

Piazzale Ospedali Civili, 1

25123 Brescia, Italy

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2 BACKGROUND: Supraglottic airway devices (SGDs) are of current use in anesthesia practice and

in emergency conditions. It has been suggested that cerebral blood flow (CBF) can decrease after

SGD insertion or cuff inflation; however, it is uncertain if this reduction is caused by the SGD or

the anesthetic drugs utilized for the anesthetic procedure. During minor surgery we separated CBF

measurements by an adequate time interval in order to measure the distinctive changes in cerebral

hemodynamics associated with anesthesia induction, SGD insertion and cuff inflation.

METHODS: Patients scheduled for minor surgery requiring general anesthesia and SGD placement

were included. Middle cerebral artery mean flow velocity (FVm-mca) and the pulsatility index (PI)

were measured through use of trans-cranial Doppler (TCD) at baseline, after anesthesia induction,

SGD insertion and cuff inflation, once a steady cardio-circulatory state was reached and end tidal

CO2 (etCO2) was within normal range.

RESULTS: A total of 21 patients were included. Following anesthesia induction, in concomitance

to a reduction in mean arterial pressure (MAP), there was a mean decrease in FVm-mca by 16.60

cm/s, p<0.005 and a mean increase in PI by 0.24, p<0.0015. MAP, FVm-mca and PI did not change

significantly, neither after SGD placement (p>0.05), nor after SGD cuffing (p>0.05).

CONCLUSION: SGD insertion and cuff inflation did not influence cerebral hemodynamics in

anesthetized patients undergoing minor surgery. At normal etCO2 range, the CBF reduction with

transient increase in PI was associated with anesthesia induction and not SGD insertion itself.

Key words: Laryngeal Mask - Carotid Artery - Transcranial Doppler Sonography - Blood Flow

Velocity

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3 Introduction

The Laryngeal Mask Airway device (LMA) was first developed by British Anesthesiologist Dr.

Archie Brain and has been in use since 1981.1 In patients with out-of-hospital cardiac arrest

(OHCA) undergoing cardiopulmonary resuscitation (CPR), although the gold standard for airway

management is represented by endo-tracheal intubation, the SGD has been used as an alternative

due to its rapid placement without the need for CPR interruption.2-6 In fact, pre-hospital

endotracheal intubation requires elevated competency, causes interruption of CPR maneuvers and,

when performed by unskilled practitioners, can produce adverse events.7,8 Yet, there is substantial

evidence showing that outcome of OHCA patients is worse when airway is managed with SGDs

than when intubated.9-11 The actual mechanism by which SGD placement could be correlated to

poor outcome is currently not known with certainty.

It has been suggested that following placement and cuff inflation this device may cause variations

in carotid artery blood flow (CABF), yet very little is known regarding its effects on cerebral

hemodynamics.12 Due to their anatomical location, the carotid arteries may be vulnerable to

increases in pressure applied within the retropharyngeal space, such as that transmitted by SGD

insertion and inflation of cuff.13-16 This in turn would cause a decrease in carotid bulb cross

sectional area, which may potentially lead to a decrease in CABF leading to variations in cerebral

blood flow (CBF).14 A recent animal model of cardiac arrest and CPR demonstrated instantaneous

reductions in CABF following placement of the SGD.17 Nevertheless, evidence regarding the

clinical consequence of the reduction in the carotid bulb cross sectional area is inconclusive, and not

all agree that the insertion of SGD may in fact induce a reduction in carotid artery section.18,19

Induction of anesthesia may cause systemic hypotension leading to variations in CBF, particularly

in patients with altered cerebrovascular autoregulation (CVA), and in the presence of intact CVA,

variations in CBF may not always directly reflect changes in arterial blood pressure (ABP) or

CABF.20,21

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4 Therefore, it is currently not clear if SGD insertion and/or cuff inflation induce significant

variations of cerebral hemodynamics in humans, or if the observed changes in CBF described in

literature are indeed caused by anesthetic drugs or coincidental systemic ventilatory variations.

We took advantage of minor elective surgical operations, where procedural times are not as

stringent as in major or emergency surgery, to separate CBF measurements by an adequate time

interval in order to measure the distinctive changes in cerebral hemodynamics and to evaluate if

these changes are associated with anesthesia induction or SGD insertion and/or cuff inflation.

COPYRIGHT© 2016 EDIZIONI MINERVA MEDICA

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5 Materials and Methods

Approval for the study, was obtained from the Local Ethics Committee on the 2nd of July, 2014 (ID-

1625 n.29) and written inform consent was obtained from all participants. The study was conducted

in the Plastic Surgery and Gastro-intestinal Endoscopy operating rooms of the Spedali Civili

university-affiliated hospital of Brescia, from July 2013 to January 2014. Patients were included if

they were 18 years of age or older, were scheduled for elective plastic or reconstructive surgery or

colonic and rectal endoscopy surgery requiring general anesthesia and SGD placement, were

hemodynamically stable with an ASA Physical Status Classification System of 2 or less, and had a

valid cranial acoustic temporal bone window for Doppler insonation. Patients with known carotid

artery disease, dysautonomic conditions that can be associated with altered CVA status either

caused by central nervous system disease (Shy-Drager syndrome, Parkinson’s disease, Lewy-body

dementia, pure autonomic failure) or peripheral nervous system disease (diabetes, amyloidosis,

Sjogren syndrome, autonomic neuropathies) were excluded from the study.22-25 All patients had the

same type of SGD, (Laryngeal Mask Airway Unique, Le Rocher, Victoria, Mahe, Seychelles)

which was placed by the same anesthesiologist . The SGD size and the cuff inflation volumes were

chosen according to those suggested by the manufacturer; size 3 SGDs (adults up to 50kg) were

inflated with 20 ml room air, size 4 (adults 50-70kg) with 30 ml and size 5 (> 70kg) with 40 ml.

The anesthesia technique was standardized using total intravenous anesthesia, and comprised

induction with propofol 1-2 mg kg-1 and fentanyl 1-2 μg kg-1, and maintenance with propofol 3-6

mg kg-1 hr -1 and remifentanyl 0.05-0.1 μg kg1 min-1. No muscle relaxants were used.

Monitoring included non-invasive ABP, heart rate (Infinity®Delta monitor, Dräger, Lübeck,

Germany), arterial oxygen saturation with pulse oximetry and end-tidal CO2 (etCO2). Mechanical

ventilation (Primus®ventilator, Dräger, Lübeck, Germany) settings were standardized so as to

maintain normal ranges in order to avoid any influence of arterial blood gases on cerebral

vasoreactivity and CBF (tidal volume 6-8ml/kg, respiratory rate set in order to maintain a etC02

between 35 - 40 mmHg and fraction of inspired oxygen at 0.35). After SGD insertion and before

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6 cuff inflation, etCO2 was immediately monitored to be sure that its value remained stable. All

patients had a clinically free airway and procedures were carried out uneventfully.

Trans-cranial Doppler measurements

In all patients studied, a 2 MHz Trans-cranial Doppler (TCD) probe (DWL Multidop®, Singen,

Germany) was used in order to measure FVm-mca as an indirect indicator of CBF, and the

pulsatility index (Peak systolic blood flow velocity - End diastolic blood flow velocity / mean

systolic blood flow velocity), as an indirect measurement of intracranial pressure (PI values > 1

were considered indicative of elevated ICP). The temporal acoustic bone window with the strongest

signal was chosen for insonation, and all exams were performed manually without continuous TCD

probe fixation. The variables were measured in four different time frames: a) basal condition, while

in the pre-anesthesia room before induction of anesthesia. Here the patient was positioned supine

and the head tilted and maintained at a 20° angle throughout the measurement in order to improve

vessel alignment; b) immediately following induction of anesthesia before SGD insertion; c) after

SGD insertion and d) after cuff inflation. Between times “c” and “d” CBF measurements were

performed only if a steady-state cardio-circulatory condition was achieved, meaning when ABP and

heart rate remained unchanged for more than 60 seconds. The TCD examiner was blinded to the

vital parameter values. Once all four TCD measurements were performed, the rest of the anesthesia

was conducted based on the judgment of the anesthesiologist.

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7

Statistical analysis

We expressed continuous variables as means and standard deviation (SD) or as medians and range

(absolute range or interquartile range [IQR]), and discrete variables as counts (percentage), unless

otherwise stated. Differences of CBF variables at various time points were analyzed by means of

repeated measurement ANOVA fitted by linear mixed models using subject as random effect.

Assuming a minimum effect size (expected difference between group means/standard deviation) of

0.7 (assumed within group standard deviation = 10) and 0.15 (SD = 0.2) respectively for FVm-mca

and PI, power 0.8 and significant level of 0.05 we estimated a sample size of 21.26 Tests were two

tailed, and p<0.05 was considered as significant. The data were analyzed with STATA 8.0 and R

(version 3.1.1 R Development Core Team, GNU General Public License).

Results

A total of 21 consecutive patients undergoing general anesthesia with SGDs were included and

studied within a time-span of three months. Surgical interventions included 12 patients who

underwent plastic surgery and 9 patients colonic and rectal endoscopy surgery.

Patient demographics, including ASA mean = 2 [range 1-3], BMI mean = 24.6 [range 20-37], age

mean = 45.6 [range 18-75], and etCO2 values post-SGD insertion and post-SGD cuffing and the

difference between the readings during these two time frames (p>0.05), are listed in Table 1. The

etCO2 ranged from 35-40 mmHg (mean 36.6 mmHg [SD 2.7]) during the measurements, and the

average cuff inflation volume was 30.7 ml (range 30-40 ml [SD 5.1]) with an average pressure of

57.4 cmH2O [SD 1.7] (range 54 – 60 cmH2O). Anesthesia induction was performed with propofol

and fentanyl, and maintenance with propofol and remifentanil in all patients.

Following anesthesia induction, there was a statistically significantly decrease in mean arterial

pressure (MAP, Figure 1a) from a baseline value of 93.5 mmHg [SD 13.8] to 66.0 mmHg after

induction [SD 9.8]; (mean decrease 27.5 mmHg [CI95% 20.9-34.2]), (p<0.005). FVm-mca also

decreased significantly from the baseline value (baseline: 54.52 cm/s [SD 16.1]; to 37.90 cm/s [SD

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8 8.3] after induction; (mean decrease 16.62 cm/s [CI95% 11.8-21.4]), (p<0.005). (Figure 1b).

Regarding the PI, however, there was a statistically significant increase following anesthesia

induction from a baseline value of 1.02 [SD 0.28], to 1.26 [SD 0.23] following anesthesia induction,

(mean increase 0.24 [CI95% 0.10-0.39]), (p=0.0015) (Figure 1c).

MAP did not change significantly after SGD placement, 66.2 mmHg [SD 10.4] (p>0.05), nor after

SGD cuffing, 66.0 mmHg [SD 10.7] (p>0.05), compared to the values measured after induction

(Figure 1a).

FVm-mca also did not change significantly after SGD placement, 35.19 cm/s [SD 7.8] (p>0.05), nor

after SGD cuffing, 37.00 cm/s, [SD 8.3] (p>0.05) (Figure 1b).

Finally, there was no significant change in PI following SGD placement (PI after anesthesia

induction 1.26 [SD 0.23], after SGD placement 1.29 [SD 0.33], or cuff inflation, 1.23 [SD 0.23]

(Figure1c). There were no significant variations in etCO2 measured immediately after SGD

placement and after cuffing (p>0.05) (Table 1).

Linear regression analysis demonstrated significant correlations between LogMFV and MAP, and

between PI and MAP, ( CI95% is represented [p<0.05]) (Figures 2a, 2b).

Discussion

We found that SGD placement and cuffing did not influence cerebral hemodynamics in patients

undergoing general anesthesia for minor elective surgery. Conversely, ABP and FVm-mca

decreased and PI increased significantly after the induction of anesthesia. Both FVm-mca and PI

correlated to the decrease in ABP. Our results suggest that the hypotension following anesthesia

induction was the true determinant of cerebral hemodynamic changes, not SGD placement or cuff

inflation itself. The induction agent used was Propofol, which causes dose dependent reduction in

systolic and diastolic ABP, cardiac output, cardiac index and systemic vascular resistance, and,

despite its ability in preserving CVA, can reduce the CBF in a substantial proportion of patients.27-30

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9 Another finding of this study was that PI increased concomitantly with the decrease in FVm-mca

and CBF. Several studies support the interpretation of PI as a reflection of the distal cerebro-

vascular resistance, attributing greater PI to higher cerebro-vascular resistance. However, PI may

also increase as a consequence of reduced cerebral perfusion pressure in animals with intact CVA,

such as during hypercapnia31. In order to exclude the influence of CO2 on PI, etCO2 was monitored

immediately following SGD placement and for the rest of the procedure. The difference in etCO2

values immediately post-SGD placement and post-SGD cuffing were not statistically significant

(Table 1). Consequently, the increase in PI was most likely caused by cerebral vasodilation

secondary to ABP reduction with secondary transient increase in cerebral blood volume and

intracranial pressure. These changes, which are transient and likely to be clinically irrelevant in

patients with good general condition and normal brain compliance, support the paradigm of

anesthetic-induced systemic hypotension with secondary cerebro-vascular modification.

In order to exclude the influence of SGD cuff pressure on FV and PI, we maintained cuff pressure

constant throughout the whole procedure at pressures suggested by the manufacturers. The

importance of SGD cuff pressure on the incidence of pharyngo-laryngeal adverse effects has been

recently underlined in a study which confronted the incidence of “pharyngo-laryngeal discomfort”

between a tight control of pressure maintained at 60 cmH2O with a second control group in whom

there were no corrections in cuff pressure but only measurements. Compared to the control group,

there was a reduction in adverse events in the group in whom the cuff pressure was maintained

constant at 60 cmH2O, although the influence on cerebral hemodynamics was not evaluated.32

Some differences compared to a few papers published previously in literature should be pointed out;

our results contradict those of Colbert SA and colleagues who showed that SGD cuff inflation

caused a reduction in the cross sectional area of the carotid artery leading to a reduction in CABF.14

In their study the time intervals used between CABF measurements were not specified, and hence,

it is not certain to what extent the reduction of CABF was due to the reduced cross section area of

the carotid artery or the hypotensive effect of the anesthetic drugs. Furthermore, it is not clear why

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10 cuff deflation lead to a significant increase of carotid cross-sectional area without any significant

variations in blood flow velocity. Compared to the study by Segal N and colleagues, who based

their study on a swine model during CCA, our study was performed in humans, and within a

general anesthesia setting.17 Another difference between the two models may be anatomical; in fact,

the human carotid arteries are found more lateral and further away from the trachea, and the

digestive tract is covered by the deep cervical fascia which may inhibit further changes in the

carotid cross section, rendering the carotid artery less vulnerable to effects caused by SGD insertion

compared to pigs.18

Limitations of the study

First, only a limited number of surgical patients in a hemodynamically stable condition were

studied; therefore, generalizing the results to other patient populations with more severe clinical

conditions such as those with cardiac arrest undergoing cardio-pulmonary resuscitation, is not

warranted. Second, cerebral blood flow velocity is not a direct measurement of CBF and depends

greatly on the radius of the middle cerebral artery that should remain constant for the measurement

to be accurate. Third, we did not test CVA before induction of anesthesia, although we carefully

excluded patients with autonomic dysfunction who are at increased risk of altered CVA alteration.

Future animal studies should replicate our model with steady-state CBF measurements rather than

CABF measurements during attempted resuscitation following cardiac arrest. If the proposed

hypothesis of anesthetic-induced systemic hypotension with induced cerebro-vascular changes

holds true, patients with intact or altered CVA should demonstrate different PI time-trends.

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11 Conclusions

SGD placement and cuffing did not influence cerebral hemodynamics in patients undergoing

general anesthesia for minor elective extracranial surgery. FVm-mca decreased and PI increased as

a consequence of the reduction in ABP following anesthesia induction. The proposed model of CBF

measurement in steady-state condition using TCD or other invasive methods should be replicated in

experimental animal settings of unstable circulatory conditions to separate the differential effects of

multiple explanatory variables of CBF reduction.

Core Messages

1) SGD placement and cuffing do not cause per se variations in cerebral hemodynamics in patients

with intact cerebrovascular autoregulation, and therefore can be safely used for airway

management during general anesthesia for extracranial surgery;

2) Drugs used for general anesthesia induction, such as propofol and remifentanil, cause a drop in

cerebral blood flow and blood flow velocity, most likely due to anesthetic-induced hypotension

and flow/metabolism coupling;

3) Anesthetic induced hypotension may cause an increase in PI in patients with intact CVA;

4) These findings warrant further investigation in patients with brain injury, at risk of having altered

cerebrovascular autoregulation, undergoing general anesthesia.

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12

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This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies (either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo, or other proprietary information of the Publisher.

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This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies (either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo, or other proprietary information of the Publisher.

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32

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This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies (either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo, or other proprietary information of the Publisher.

Chantzara G, Stroumpoulis K, Alexandrou N, Kokkinos L, Iacovidou N, Xanthos T.

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16 TITLE OF TABLE

Table 1. Patients ASA (American Society of Anesthesiology physical status classification

system), BMI (body mass index), age, etCO2 (end tidal carbon dioxide in mmHg)

values post-SGD insertion and post-SGD cuffing (p > 0.05). The last column showing

the differential values between the two etCO2 time frame measurements.

TITLES OF FIGURES

Figure 1a,1b,1c. Box-Plot representation of the variations in *MAP, **MFV and***PI, before and

after anesthesia induction of (1a-1b), after †SGD insertion (c) and after SGD cuff inflation. The

only statistically significant variation in these parameters took place following anesthesia induction

(p<0.05). The boxes display the 1st and 3rd quartiles, while the whiskers correspond to the

maximum and minimum value of each parameter during the four time frames. The median is

represented by the horizontal line inside the box. *MAP (mean arterial pressure), **MFV (mean flow velocity), ***PI (pulstality index), †SGD (Supraglottic airway device) .

Figure 2a, 2b. Linear regression analysis showing the correlations between LogMFV and MAP (a),

and between PI and MAP (b), (CI95% is represented). (p<0.05).

Authors’ contributions

FR was involved in all aspects of the study from conception and design, to data collection

and analysis, to preparation of the manuscript. NZ, AT, FP, SP, NF were involved during

data collection, SC SP and NF were involved in data analysis. NL was also involved in all

aspects of the study as senior author from conception and design, to data collection and

analysis, to preparation of the manuscript.

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Patient Number

ASA BMI (Kg/m2)

AGE etCO2 (mmHg) Differential etCO2

(mmHg) Post-SGD insertion

Post-SGD cuffing

1 2 23 18 36 37 1

2 1 22 38 36 36 0

3 2 31 46 37 36 -1

4 1 25 18 38 40 2

5 2 24 38 40 40 0

6 2 23 18 40 39 -1

7 2 22 52 38 38 0

8 2 20 37 35 36 1

9 2 24 52 38 39 1

10 2 37 60 36 35 -1

11 2 30 63 34 32 -2

12 2 25 68 36 34 -2

13 2 26 65 32 33 1

14 2 24 65 40 38 -2

15 2 23 42 38 38 0

16 1 20 43 32 33 1

17 2 26 41 40 39 -1

18 2 21 47 36 36 0

19 2 22 75 35 34 -1

20 2 24 50 37 37 0

21 2 25 22 38 36 -2

Table 1. Patients ASA (American Society of Anesthesiology physical

status classification system), BMI (body mass index), age, etCO2 (end

tidal carbon dioxide in mmHg) values post-SGD insertion and post-SGD

cuffing (p > 0.05). The last column showing the differential values between

the two etCO2 time frame measurements.

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